What is pneumocystis?

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Pneumocystis is a fungus that lives in the lungs of mammals, including humans, in a parasitic relationship. It causes no disease and does no harm unless the mammal’s immune system becomes suppressed by medications, age (very young and very old), disease (such as acquired immunodeficiency syndrome), pregnancy, malnutrition, chemotherapy, leukemia, or organ transplant.
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Definition

Pneumocystis is a fungus that lives in the lungs of mammals, including humans, in a parasitic relationship. It causes no disease and does no harm unless the mammal’s immune system becomes suppressed by medications, age (very young and very old), disease (such as acquired immunodeficiency syndrome), pregnancy, malnutrition, chemotherapy, leukemia, or organ transplant.

Natural Habitat and Features

Pneumocystis species are either oval or cup-shaped, and they have a thick cell wall. These larger cells usually contain eight spores. The trophozoite cells are smaller and look like ameba. They have a thin cell wall. Pneumocystis cells blend in with the alveolar cells unless a stain is applied to the specimen. There is limited information about the appearance of Pneumocystis species cells.

Pneumocystis species require a host to live and reproduce. They cannot be grown in a culture medium. They do not appear to be present in the environment. Although hundreds of species of Pneumocystis are thought to exist, only five have been named: jirovecii, which lives in humans; murina, which lives in mice; wakefieldiae and carinii, which both can live in rats; and oryctolagi, which lives in rabbits. These species are found only in their related mammal and do not cross-contaminate other types of mammals.

Pneumocystis species find their way into the lungs of their respective mammal early in life. In humans, jirovecii inhabits the lungs of a child during his or her first year of life. In other mammals, such as the rat, carinii is found in the lungs of newborns within hours of delivery. Humans and other mammals do produce antibodies to their respective Pneumocystis species.

The life cycle of Pneumocystis species is not completely known. Most of the available information about Pneumocystis species has come from studying carinii in lab rats. It is thought that Pneumocystis reproduces by two means: mitosis and sexual reproduction. Trophic forms of the fungus reproduce by replicating their genetic material and then splitting into two. Trophic cells provide nutrition for other cells. In sexual reproduction, two haploid cells merge to produce a zygote or sporocyte. Haploid cells are cells that contain one-half of the necessary genetic material. The zygote produces four haploid nuclei by splitting its genetic material, and then, by mitosis, the zygote produces eight haploid nuclei. The zygote cell then packages the eight nuclei into eight double-walled spores. The spores are released from the zygote cell and are capable of both asexual and sexual reproduction. It is not known how the spores are released from the lung.

Pathogenicity and Clinical Significance

In the healthy, immune-competent mammal, Pneumocystis appears to be a benign parasite. There appears to be a delicate balance of normal host function and normal fungus replication as long as the host’s immune system remains strong. The mammal’s immune system does not attack the Pneumocystis because of its surface antigens, and the Pneumocystis does not invade its host. Airborne transmission of Pneumocystis does not generally cause disease. Disease arises from the Pneumocystis that already resides within the mammal.

When a Pneumocystis infection occurs, it almost always develops in the lungs. When the host’s immune system becomes weakened, the Pneumocystis cells increase in number and are said to colonize the lung. Within the alveoli of the lung, the Pneumocystis trophic cells cling to the epithelial cells in the alveoli. The immune system of the host attempts to fight the emerging infection by instituting the inflammatory response, a mechanism for responding to cellular damage. In the inflammatory response, the area is flooded with white blood cells, particularly the neutrophils and lymphocytes, and the white blood cells called macrophages; tumor necrosis factor, which regulates immune cells, also plays a major role. The inflammatory response causes more damage to the alveoli than does the Pneumocystis. The inflammatory response damages the alveolar tissue and interferes with oxygen and carbon dioxide exchange in the lungs.

In the immune compromised person, the T cells may be absent or decreased, but still, the alveoli fill with thick, white fluid. Pneumocystis pneumonia is a serious condition with a mortality rate of between 30 and 50 percent. Sometimes, persons using immune suppressing drugs will be given a medication to prevent pneumocystis pneumonia.

Drug Susceptibility

The treatment of choice for pneumocystis pneumonia is trimethoprim-sulfamethoxazole, which can be administered orally or intravenously. Other antibiotics or medications against protozoa, including Pneumocystis, include pentamidine, dapsone, primaquine plus clindamycin, and atovaquone. There have been some reports of Pneumocystis resistance to trimethoprim-sulfamethoxazole. Corticosteroids may be administered during the first seventy-two hours of pneumocystis pneumonia treatment to depress lung inflammation.

Bibliography

AIDS InfoNet. “Pneumocystis Pneumonia (PCP).” Available at http://www.aidsinfonet.org.

Cushion, Melanie T. “Are Members of the Fungal Genus Pneumocystis (a) Commensals; (b) Opportunists; (c) Pathogens; or (d) All of the Above?” PLoS Pathogens 6 (September 23, 2010). Available at http://www.plospathogens.org.

Van Oosterhout, Joep J. G., et al. “Pneumocystis Pneumonia in HIV-Positive Adults, Malawi.” Emerging Infectious Diseases 13 (2007): 325-328.

West, John B. Pulmonary Pathophysiology: The Essentials. 7th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008.

Wilkin, Aimee, and Judith Feinberg. “ Pneumocystis carinii Pneumonia: A Clinical Review.” American Family Physician 60 (October 15, 1999): 1699-1714. Also available at http://www.aafp.org/afp/991015ap/ 1699.html.

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